cells. We will perform microarray, epigenotyping, and bioinformatic analysis of these clones, fully reprogrammed human ES cell-like cells, wild type human ES cells, and mesenchymal and myeloid cells to offer insights into reprogramming to a pluripotent state and into cell fate changes to other lineages. This project will result in a significant improvement in our understanding of how the developmental status of differentiated cells can be altered. Reprogramming the genome from a somatic cell to a pluripotent state would be useful to generate patient-specific ES cells, thus overcoming the problem of tissue rejection resulting from genetic mismatches between donor and recipient. Perhaps more importantly, understanding how to reprogram differentiated cells to entirely new fates may ultimately lead to novel regenerative therapies that act on patients' endogenous cells in the absence of cell transplantation. This project represents an important early step in that direction.